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Qwin analysis system

Manufactured by Leica
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The Qwin analysis system is a digital imaging solution designed for microscopy applications. It provides tools for image capture, processing, and analysis. The system supports a range of microscopy techniques and enables users to perform quantitative measurements and evaluations on digital microscopic images.

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Lab products found in correlation

Kaiser s glycerol gelatine, by Merck Group (2 mentions)

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Qwin image analysis system (15 citations) Qwin Proimage analysis system (3 citations) Qwin-based analysis system (2 citations) Qwin image processing and analysis system (2 citations)

4 protocols using qwin analysis system

1

Quantification of IL-17 Expression in PsA

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Quantification of IL-17A-, IL-17F-, IL17RA- and IL-17RC-expressing cells in PsA skin and synovial tissues was performed by computer-assisted image analysis, as previously described [29 (link)]. Briefly, after immunohistochemical staining, all coded sections (one section per patient per time-point) were randomly analyzed (18 high-power fields from different parts of the section were analyzed; the mean of the 18 high-power fields was calculated). The images of the high-power fields were analyzed using the Qwin analysis system (Leica, Cambridge, UK). The expression of stained proteins was calculated for each section as the median integrated optical density (IOD)/mm2 [33 (link)].
Bolt J.W., van Kuijk A.W., Teunissen M.B., van der Coelen D., Aarrass S., Gerlag D.M., Tak P.P., van de Sande M.G., Lebre M.C, & van Baarsen L.G. (2022). Impact of Adalimumab Treatment on Interleukin-17 and Interleukin-17 Receptor Expression in Skin and Synovium of Psoriatic Arthritis Patients with Mild Psoriasis. Biomedicines, 10(2), 324.
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2

Immunohistochemical Analysis of CSF-1, IL-34, and CD68

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Serial sections from six different TissueTek-embedded biopsy samples per patient were cut with a cryostat (5 μm), fixed with acetone, and endogenous peroxidase activity blocked with 0.3 % hydrogen peroxide in 0.1 % sodium azide/phosphate-buffered saline. Sections were stained overnight at 4°C with Abs against CSF-1 (R&D), IL-34 (M4, provided by Five Prime Therapeutics Inc.) and CD68 (Dako). Equivalent concentrations of irrelevant mouse monoclonal Abs were used as negative controls. Sections were then washed and incubated with goat anti-mouse-horseradish peroxidase (HRP) (Dako), except in the case of anti-IL-34 Ab, which was followed by incubation with biotinylated tyramide and streptavidin-HRP. Sections were developed with amino-ethylcarbazole (AEC, Vector Laboratories), counterstained with Gill’s hematoxylin (Klinipath), and mounted in Kaiser’s glycerol gelatine (Merck). Stained sections were analyzed by computer-assisted image analysis using the Qwin analysis system (Leica) as previously described in detail [42 (link)]. Values of integrated optical densities (IOD)/mm2 were obtained and corrected for the total number of nuclei/mm2. Data were presented as the number of positive cells/mm2 for quantitative analysis of cell-type-specific markers.
Garcia S., Hartkamp L.M., Malvar-Fernandez B., van Es I.E., Lin H., Wong J., Long L., Zanghi J.A., Rankin A.L., Masteller E.L., Wong B.R., Radstake T.R., Tak P.P, & Reedquist K.A. (2016). Colony-stimulating factor (CSF) 1 receptor blockade reduces inflammation in human and murine models of rheumatoid arthritis. Arthritis Research & Therapy, 18, 75.
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3

Histological Evaluation of Liver Damage

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Liver tissue was fixed in 10% formalin and was embedded in paraffin. Tissue sections were cut at 4 µm, mounted on slides, stained with hematoxylin and eosin (H&E) for general liver structure, Periodic Acid Schiff (PAS) to demonstrate the glycogen deposition in hepatocytes and Kupffer cells. The liver damage was semi quantitatively assessed as follows; sinusoidal congestion, and loss of the glycogen deposition in hepatocytes. The sinusoidal congestion, and glycogen loss were scored between 0–3; 0 was defined as normal liver, 1 was defined as liver damage involving ≤25% of liver, 2 was defined as liver damage involving 25–50% of liver and 3 was defined as liver damage involving ≥50% of liver. For each criterion, ten fields were examined in X20 objective magnification. In addition, Kupffer cells were counted manually on digital images Leica Q Win analysis system using point counting. For each animal, three sections were used. In each section, 10 fields were randomly chosen at 40X, totaling 30 fields per animal.
Bilgic Y., Akbulut S., Aksungur Z., Erdemli M.E., Ozhan O., Parlakpinar H., Vardi N, & Turkoz Y. (2018). Protective effect of dexpanthenol against cisplatin-induced hepatotoxicity. Experimental and Therapeutic Medicine, 16(5), 4049-4057.
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4

Quantitative Immunohistochemical Analysis of Protein Acetylation

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Serial sections from TissueTek-embedded biopsy samples were cut with a cryostat (5 μm), fixed with acetone and endogenous peroxidase activity blocked with 0.3% hydrogen peroxide in 0.1% sodium azide/phosphate-buffered saline.27 (link) Sections were stained overnight at 4°C with rabbit antibodies against acetylated lysine (acLys) or acetylated histone 3(Lys18) (acH3) (both from Cell Signaling Technology). Equivalent concentrations of control rabbit antibodies (anti-fluorescein isothiocyanate, Thermo Scientific) were applied for control sections. Sections were then washed and incubated with horseradish peroxidase (HRP)-conjugated swine anti-rabbit antibodies (Dako), followed by incubation with biotinylated tyramide and streptavidin-HRP, and development with amino-ethylcarbazole (AEC, Vector Laboratories). Sections were subsequently counterstained with Gill’s haematoxylin (Klinipath) and mounted in Kaiser’s glycerol gelatine (Merck). For quantitative analysis of protein acetylation, stained sections were randomly coded by an independent observer, blinded to antibodies used and clinical diagnosis. Stained slides were analysed by computer-assisted image analysis using the Qwin analysis system (Leica) as previously described.28 (link) Values of integrated optical densities (IOD)/mm2 were obtained and corrected for total number of nucleated cells per square millimetre.
Angiolilli C., Grabiec A.M., Ferguson B.S., Ospelt C., Fernandez B.M., van Es I.E., van Baarsen L.G., Gay S., McKinsey T.A., Tak P.P., Baeten D.L, & Reedquist K.A. (2014). Inflammatory cytokines epigenetically regulate rheumatoid arthritis fibroblast-like synoviocyte activation by suppressing HDAC5 expression. Annals of the rheumatic diseases, 75(2), 430-438.
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